TY - JOUR
T1 - Risk of Cardiovascular Conditions in Patients with Chronic Hypoparathyroidism
T2 - A Retrospective Cohort Study
AU - Gosmanova, Elvira O.
AU - Chen, Kristina
AU - Ketteler, Markus
AU - Rejnmark, Lars
AU - Mu, Fan
AU - Swallow, Elyse
AU - Briggs, Allison
AU - Sherry, Nicole
AU - Kaul, Sanjiv
N1 - Funding Information:
This research and the journal’s Rapid Service and Open Access fees were funded by Shire Human Genetic Therapies, Inc., a Takeda company, Lexington, MA, USA. All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship for this article, take responsibility for the integrity of the work as a whole, and have given their approval for this version to be published. KC, FM, ES, AB and NS contributed to the conception and design of the research. KC, FM, ES, and AB contributed to the acquisition and analysis of data. All authors (EOG, KC, MK, LR, FM, ES, AB, NS, and SK) contributed to the interpretation of the data, drafting of the manuscript, critical revision of the manuscript, agree to be fully accountable for ensuring the integrity and accuracy of the work, and read and approved the final manuscript. Under the direction of the authors, writing and editorial support in the preparation of this manuscript was provided by Alan Storey, PhD, an employee of ICON (Marlow, Buckinghamshire, UK), and funded by Shire Human Genetic Therapies, Inc., a Takeda company, Lexington, MA, USA. Elvira O. Gosmanova has served as a consultant for Shire, a Takeda company. Kristina Chen is a former employee of Shire Human Genetic Therapies, Inc., a Takeda company, Lexington, MA, USA; current affiliation is Arena Pharmaceuticals, Boston, MA, USA. Markus Ketteler has served as a research investigator and consultant for Shire, a Takeda company. Lars Rejnmark has served as a consultant and speaker for Shire, a Takeda company. Fan Mu, Elyse Swallow are employees, and Allison Briggs is a former employee of Analysis Group, Inc. contracted by Shire, a Takeda company, to conduct this research. Nicole Sherry is a former employee of Shire Human Genetic Therapies, Inc., a Takeda company, Lexington, MA, USA. Sanjiv Kaul has served as an advisory board member for Ultromics and as a consultant for Shire, a Takeda company. Elvira O. Gosmanova is an employee of the US Department of Veterans Affairs. Opinions expressed in this article are those of the authors and do not necessarily represent the opinion of the US Department of Veterans Affairs. Because this study used de-identified licensed data from a HIPAA-compliant managed care database, ethics committee approval and informed consent were not required. The datasets generated and/or analyzed during the current study from the managed care claims database are not publicly available but are available from the corresponding author on reasonable request. Initial data from this study were presented at the Endocrine Society Annual Meeting; March 23–26, 2019, New Orleans, LA, USA; and at the 21st European Congress of Endocrinology; May 18–21, 2019, Lyon, France.
Funding Information:
This research and the journal’s Rapid Service and Open Access fees were funded by Shire Human Genetic Therapies, Inc., a Takeda company, Lexington, MA, USA.
Publisher Copyright:
© 2021, The Author(s).
PY - 2021/8
Y1 - 2021/8
N2 - Introduction: In patients with chronic hypoparathyroidism disordered calcium homeostasis has been associated with risk of cardiovascular diseases, including cardiomyopathy, congestive heart failure, and arrhythmia; however, larger-scale studies are needed to examine these risks. This study evaluated the risk of cardiovascular conditions among patients with chronic hypoparathyroidism. Methods: Adults with and without chronic hypoparathyroidism were selected from a medical insurance claims database in the USA from January 2007 to June 2017, and were followed for up to 5 years. Associations between chronic hypoparathyroidism and incident atrial fibrillation (AF), tachyarrhythmia, myocardial infarction (MI), coronary artery disease (CAD), heart failure (HF), stroke, cerebrovascular disease, peripheral vascular disease (PVD), and a combined cardiovascular endpoint of cerebrovascular disease, CAD, HF, and PVD were compared between cohorts using Kaplan–Meier analyses and unadjusted and adjusted Cox proportional hazards models. Results: In 8097 patients with chronic hypoparathyroidism compared with 40,485 patients without, respectively, mean ± SD ages were 58.6 ± 16.3 and 47.3 ± 18.0 years, 76.2% and 54.4% were female, and 19.4% and 9.5% had the combination of cardiovascular findings at baseline. In adjusted analyses, patients with chronic hypoparathyroidism had significantly higher risk (adjusted hazard ratio and 95% confidence interval) of incident AF (1.72; 1.51–1.97), tachyarrhythmia (1.68; 1.32–2.14), MI (1.18; 1.01–1.38), CAD (1.39; 1.26–1.54), HF (1.64; 1.46–1.84), stroke (1.45; 1.31–1.62), cerebrovascular disease (1.48; 1.34–1.62), PVD (1.66; 1.51–1.81), and combined cardiovascular endpoint (1.63; 1.52–1.75), all P < 0.001 except P = 0.036 for MI, compared with patients without chronic hypoparathyroidism. Conclusions: This large retrospective cohort study showed that chronic hypoparathyroidism was associated with increased risk of incident cardiovascular conditions and arrhythmias. Results should be evaluated in light of limitations inherent to claims database analyses. Further studies are warranted to investigate reasons for these risks and to develop strategies for reducing cardiovascular conditions in patients with chronic hypoparathyroidism.
AB - Introduction: In patients with chronic hypoparathyroidism disordered calcium homeostasis has been associated with risk of cardiovascular diseases, including cardiomyopathy, congestive heart failure, and arrhythmia; however, larger-scale studies are needed to examine these risks. This study evaluated the risk of cardiovascular conditions among patients with chronic hypoparathyroidism. Methods: Adults with and without chronic hypoparathyroidism were selected from a medical insurance claims database in the USA from January 2007 to June 2017, and were followed for up to 5 years. Associations between chronic hypoparathyroidism and incident atrial fibrillation (AF), tachyarrhythmia, myocardial infarction (MI), coronary artery disease (CAD), heart failure (HF), stroke, cerebrovascular disease, peripheral vascular disease (PVD), and a combined cardiovascular endpoint of cerebrovascular disease, CAD, HF, and PVD were compared between cohorts using Kaplan–Meier analyses and unadjusted and adjusted Cox proportional hazards models. Results: In 8097 patients with chronic hypoparathyroidism compared with 40,485 patients without, respectively, mean ± SD ages were 58.6 ± 16.3 and 47.3 ± 18.0 years, 76.2% and 54.4% were female, and 19.4% and 9.5% had the combination of cardiovascular findings at baseline. In adjusted analyses, patients with chronic hypoparathyroidism had significantly higher risk (adjusted hazard ratio and 95% confidence interval) of incident AF (1.72; 1.51–1.97), tachyarrhythmia (1.68; 1.32–2.14), MI (1.18; 1.01–1.38), CAD (1.39; 1.26–1.54), HF (1.64; 1.46–1.84), stroke (1.45; 1.31–1.62), cerebrovascular disease (1.48; 1.34–1.62), PVD (1.66; 1.51–1.81), and combined cardiovascular endpoint (1.63; 1.52–1.75), all P < 0.001 except P = 0.036 for MI, compared with patients without chronic hypoparathyroidism. Conclusions: This large retrospective cohort study showed that chronic hypoparathyroidism was associated with increased risk of incident cardiovascular conditions and arrhythmias. Results should be evaluated in light of limitations inherent to claims database analyses. Further studies are warranted to investigate reasons for these risks and to develop strategies for reducing cardiovascular conditions in patients with chronic hypoparathyroidism.
KW - Arrhythmia
KW - Cardiovascular disease
KW - Chronic hypoparathyroidism
KW - Retrospective cohort study
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U2 - 10.1007/s12325-021-01787-7
DO - 10.1007/s12325-021-01787-7
M3 - Article
C2 - 34165700
AN - SCOPUS:85111958981
VL - 38
SP - 4246
EP - 4257
JO - Advances in Therapy
JF - Advances in Therapy
SN - 0741-238X
IS - 8
ER -